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Biomedical subjects

S Sevitt

Publications and source records attributed to S Sevitt.

At least 19 recordsLinked to original sources
PubMed1986

Atherosclerotic lesions from the reduction of pulmonary emboli.

Seventy-five intimal arterial thickenings (from 58 subjects) related to pulmonary emboli were examined. Many showed residua derived from the emboli (fibrin, platelets, haemosiderin) and proliferation of elastica and smooth muscle cells. Features resembling those of atherosclerosis were the frequent presence of extracellular lipid and apolipoprotein-B containing lipoproteins (LpB) which corresponded closely in distribution; and (in about 40% of the thickenings) collections of fat-filled (foam) cells. Platelet antigens were often detected within foam cells in some cases, in company with LpB. The results indicate that at least some intimal thickenings originating from pulmonary emboli undergo transformation to atherosclerotic plaques. The role of pulmonary hypertension in the process was investigated. Mechanisms relevant to this transformation and to theories of atherogenesis are discussed.

Adolescent↗
PubMed1986

Platelets and foam cells in the evolution of atherosclerosis. Histological and immunohistological studies of human lesions.

Sixty-seven coronary, aortic and other lesions (39 subjects) ranging from minor to advanced disease were studied histologically and by immunohistology for antigens of platelets, beta-lipoprotein (LpB) and fibrinogen. Collections of lipid-filled foam cells were found in nearly every lesion mainly in the thickened intima, sometimes associated with macrophages. Foam cells were also present elsewhere including, in advanced lesions, necrotic zones filled with cholesterol needles. Then they too were necrotic. Platelets were observed in many lesions as small free clusters and/or phagocytosed in foam cells and sometimes also in macrophages. Cellular and extracellular reactions for platelet derivatives and for LpB were very frequent. Reactions for fibrinogen were only extracellular. Foam cell cytoplasm reacted for platelet derivatives and for LpB whilst macrophages, endothelium and certain other cells sometimes reacted for platelet derivatives but rarely for LpB. The studies indicate that: Foam cells originate from macrophages mainly in the intima and many migrate elsewhere. Their formation and their uptake of LpB requires cellular acquisition of a platelet factor or factors. Acquisition of platelet factor(s) is by phagocytosis of intact platelets and/or uptake of extracellular soluble derivatives from disrupted platelets. These processes begin early, are likely to be continuous and are significant for the evolution of atherosclerosis including the necrotic foci of advanced lesions.

Antigens↗
PubMed1979

A review of the complications of burns, their origin and importance for illness and death.

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.

Burns↗
PubMed1978

Pathology of injury: some problems and new horizons.

The pathology of trauma is a relatively neglected subject with promise of new horizons. The neglect is a matter of concern for academic and practical needs, including the basis of therapeutic progress. Many problems await solution and a few of these are discussed. Some of the recommendations made by the Working Party of the Royal College of Pathologist on the Pathology of Injury are summarized.

Acute Kidney Injury↗
PubMed1977

The mechanisms of traumatic rupture of the thoracic aorta.

This paper reviews evidence and ideas on closed accidental rupture of the aorta, and refers to an analysis of 37 subjects in whom traumatic aortic ruptures were found at necropsy. The mechanisms of rupture of the ascending aorta and the proximal and distal parts of the descending aorta are discussed. Aortic rupture is one of the major causes of rapid death after traffic accidents, especially in occupants of motor vehicles. However, about 20 per cent of subjects survive for hours, days or longer after the accident, allowing time for surgical repair in some cases.

Accidents, Traffic↗
PubMed1977

Organic fragmentation in pulmonary thrombo-emboli.

Organic fragmentation is a cell-mediated process whereby the periphery of thrombo-emboli is broken up into multiple tiny fragments lined by flat cells and separated by endothelialised clefts and spaces. The process was looked for in 238 lung emboli from 107 subjects and was observed in 45 emboli (41 subjects). The true incidence is much higher since fragmentation is preceded by the surfacing of emboli by flat endothelial cells. Among such emboli its frequency was 41%. Fragmentation can involve emboli of all sizes though it is most frequent and extensive in small ones. The process is important for the resolution of emboli and helps the canalisation of the embolised arteries. It reduces the size of emboli and may also undermine mural attachments and thereby lessen the extent of anchoring to the vessel wall. The mechanism of fragmentation and the origin of the cells responsible are discussed.

Adolescent↗
PubMed1976

Arterial wall lesions after pulmonary embolism, especially ruptures and aneurysms.

During an histological study of pulmonary thromboembolism, arterial wall splits, many associated with saccular microaneurysms, were observed in association with emboli or their fibrous residue. Other aneurysmal lesions, non-inflammatory focal medial necrosis, and medial scars were also seen in a few cases. The nature of the arterial rents indicates that they arose by mechanical splitting after acute stretching of the artery at the time of embolic impaction. Saccular aneurysms then developed in some. Impaction could also have caused the foci of medial necrosis while the medial scars could represent healed former necrosis of rupture. Though the observed incidence of lesions was relatively low, this seems to be due to their small sizes and the sampling inherent in conventional histological analysis. It is concluded that arterial splits are probably a common effect of pulmonary embolism and often give rise to small aneurysms.

Adolescent↗
PubMed1975

Hypoxaemia after fractures.

Serial arterial blood-gas analyses showed a phase of primary hypoxaemia in thirty-two out of fifty fracture patients (64 per cent) without head, chest or abdominal injury. The incidence was greater in those with shaft fractures of the femur or tibia or both, than in those with fractured hips, and was related to the severity of injury and the nature of the accident. Most affected subjects were already hypoxaemic on admission to hospital; the arterial PO2 commonly fell to between 60 and 70 millimetres of mercury, and the episode generally lasted a few days. The hypoxaemia was generally subclinical but four patients developed mild fat embolism. Early hypoxaemia was not found in six patients admitted with only soft-tissue injuries. One or more subsequent attacks of subclinical hypoxaemica, each lasting a few days, occurred in half of those previously affected. Most episodes followed fracture operation or manipulation. Pulmonary thromboembolism seemed responsible in two patients, but it could be excluded in others given oral anticoagulant prophylaxis from soon after admission. Pulmonary fat embolism is the most likely explanation of the primary episodes and could account for most of the subsequent periods of hypoxaemia.

Accidents, Traffic↗
PubMed1974

Diffuse and focal oxygen pneumonitis. A preliminary report on the threshold of pulmonary oxygen toxicity in man.

Utilizing hyaline membranes and proliferative pneumonitis as evidence of pulmonary oxygen toxicity, the lung changes in 21 patients (19 injured, two inhaled smoke) who died after oxygen therapy are correlated with the intensity and duration of oxygen administration. Diffuse pneumonitis inducing hypoxaemia was found in 10 (or 11) subjects, and in nine of them it was associated with the breathing of high concentrations of oxygen (60 to 100%) for at least two days. In at least eight subjects the pneumonitis contributed to death, and two others who survived for weeks had extensively fibrosed lungs. The breathing of 40% oxygen for a sufficient time seems to be a threshold for dangerous lung effects, since one patient developed a diffuse pneumonitis and another a partly-diffuse partly-focal pneumonitis while exposed to this concentration. Those respiring oxygen concentrations between 25 and 40% for days developed either subclinical focal lung lesions or had no relevant lung changes.

Adolescent↗
PubMed1974

The structure and growth of valve-pocket thrombi in femoral veins.

The structure of 50 small thrombi in femoral valve pockets and the microscopic contents of 35 apparently empty pockets were studied in an attempt to ascertain the nature of the microscopic nidi from which thrombi form and their manner of growth to visible thrombi. Sixteen thrombi had little or no cellular invasion. Most of these recent structures had two main regions, red areas restricted distally in the pocket by the vein wall, and larger white regions comprising most of the thrombus length and often covering the red areas. Red areas are the early sites of cellular adhesion and invasion and the likely sites of origin of most thrombi. They were usually dominated by red cells and fibrin. White zones, which represent propagation growth, are characterized by many foci of platelets with fibrin borders (platelet-fibrin units). Some red areas also contained platelet-fibrin units but they were few and tiny; platelets were not seen in others and one small wholly red thrombus was devoid of platelets. Degenerative changes in platelet-fibrin units were observed, and it is postulated that many become purely fibrin structures. There was no significant evidence of preceding intimal damage in the vein wall. Therefore nidi are laid down on normal endothelium probably on the vein wall near the apex of the pocket. Some pockets, empty of thrombi, contained condensed foci of red cells or tiny fibrin fragments surfaced by endothelial cells and considered to be the remnants of aborted thrombi; a few contained clumps of platelets or leucocytes. It is postulated that any of these may represent the nidi from which thrombi grow. Several thrombi also incorporated large fat droplets, numerous in two. Fat embolic globules derived from fractures are their likely source.

Aged↗